Project description:Collectively, viruses are the principal cause of cancers arising in patients with immune dysfunction, including HIV+ patients. Kaposi’s Sarcoma (KS) etiologically linked to KSHV continues to be the most common AIDS-associated tumor. The involvement of oral cavity represents one of the most common clinical manifestations of this tumor. HIV infection incurs an increased risk for periodontal diseases and oral carriage from a variety of pathogenic bacteria. In the current study, by using 16S rRNA based pyrosequencing, we found that oral shedding of KSHV altered oral microbiota signature in HIV+ patients which may contribute to virus-associated malignancies development.
Project description:Salmonella species infect many vertebrate species, and pigs colonized with Salmonella enterica serovar Typhimurium (ST) are usually asymptomatic, making detection of these Salmonella-carrier pigs difficult. The variable fecal shedding of this gram-negative bacteria in such pigs is an important cause of foodborne illness and zoonotic disease. To investigate gene pathways and biomarkers associated with the variance in Salmonella shedding following experimental inoculation, we have initiated the first analysis of the whole blood transcriptional response induced by Salmonella. A population of pigs (n=40) was inoculated with ST and the peripheral blood and feces were collected between 2 and 20 days post-inoculation. Two groups of pigs with either low shedding (LS) or persistent shedding (PS) phenotypes were identified. The global transcriptional changes in response to ST inoculation were identified by Affymetrix Genechip?analysis of peripheral blood RNA at day 0 and day 2 post-inoculation. Forty pigs (n=40) was inoculated with ST. Four low shedding (LS) pigs and six persistent shedding (PS) pigs were identified. Transcriptom of peripheral blood collected at 0 and 2 dpi were identified by Affymetrix Genechip analysis.
Project description:The p53 gain of function p53R172H promotes accelerated tumor growth and progression to carcinoma. To identify gene expression changes associated with the oncogenic function of mutant p53 we compared the expression profiles of oral tumors induced by activation of oncogenic K-ras and p53 gain- or loss-of-function mutations Oral tumors were induced by activation of endogenous oncogenic K-rasG12D and p53 loss- or gain-of-function mutations (p53R172H) Oral tumors from mice carrying the p53R172H mutation or deletion of p53 were collected for gene expression analysis
Project description:Shisha smoking has been epidemiologically linked to development of oral lesions as well as various cancers. However, few molecular studies investigate the pathobiology of shisha induced cancer. In this study we investigate the effects of chronic shisha exposure in an in vitro model using normal, immortalized, non-transformed oral keratinocytes. Quantitative proteomic and phosphoproteomic analyses were performed on OKF6/TERT1 cells exposed to shisha for a period of 8 months. Gene Ontology and pathway analysis of dysregulated proteins and phosphoproteins were carried out to identify significantly enriched biological processes and pathways in shisha exposed cells compared to parental cells. Chronic shisha exposure resulted in increased cell scattering phenomenon in OKF6/TERT1 cells. Quantitative data analysis revealed differential phosphorylation of 164 phosphopeptides (fold change ≥1.5, p≤0.05) corresponding to 136 proteins. Kinases such as PRKCD were seen to be hyperphosphorylated. Pathway analysis revealed an enrichment of hyperphosphorylated and/or overexpressed proteins involved in the mTORC1 and EIF4F complexes. These complexes are associated with initiation of protein translation and are known to the affected in cancers. Network analysis also highlighted a downregulation of proteins associated with Type I interferon signaling in shisha exposed cells. High throughput phosphoproteomic analysis revealed global perturbations to the molecular milieu of oral keratinocytes upon shisha exposure. Further studies are needed to validate putative targets in oral cancer patients with shisha smoking history.
Project description:A comparative transcriptome analysis was performed to compare the fruit AZs of the non-shedding E. oleifera variant and from an individual of the same progeny that sheds its ripe fruit normally. The study provides evidence for widespread perturbation to gene expression in the AZ of the non-shedding variant, compared to the normal fruit-shedding control, and allows insight into abscission related functions.
Project description:The p53 gain of function p53R172H promotes accelerated tumor growth and progression to carcinoma. To identify gene expression changes associated with the oncogenic function of mutant p53 we compared the expression profiles of oral tumors induced by activation of oncogenic K-ras and p53 gain- or loss-of-function mutations Oral tumors were induced by activation of endogenous oncogenic K-rasG12D and p53 loss- or gain-of-function mutations (p53R172H)
Project description:To further development of gene expression approach to squamous carcinoma, we have employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential to reveal the relation between oral squamous carcinoma (OSCC) and human normal oral mucosal epithelial keratinocytes.
Project description:Due to betel nut chewing habit, oral cancer is the fourth leading cause of cancer death among Taiwanese men. In addition, oral cancer is the most common malignancy observed in men with 25-44 years old, alerting an urgent need to curb this disease. It is hypothesized that betel nut ingredients exhibit carcinogenic effects on the oral epithelium and alter local immune system. As a step to identify potential oncogenic gene fusions in Taiwanese oral cancer cells, total RNAs of two immortalized oral keratinocytes (CGHNK2, -K6) and five oral squamous cell carcinoma cell lines (C9, OC3, OEC-M1, TW2.6) were subjected to RNA-sequencing analysis, followed by an in-house bioinformatic pipeline for fusion gene detection.